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Pivotal Advance: PKCζ is required for migration of macrophages
Author(s) -
Guo Hua,
Ma Yongjie,
Zhang Baogang,
Sun Baocun,
Niu Ruifang,
Ying Guoguang,
Zhang Ning
Publication year - 2009
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0708429
Subject(s) - chemotaxis , biology , protein kinase c , microbiology and biotechnology , cofilin , cell migration , cancer research , metastasis , cancer cell , kinase , cell culture , cancer , cell , actin cytoskeleton , receptor , cytoskeleton , biochemistry , genetics
The crosstalk, mediated by chemoattractants, between cancer cells and tumor‐associated macrophages, plays an important role in tumor invasion and metastasis. Our previous study reported that atypical protein kinase C ζ (PKCζ) regulates epidermal growth factor‐induced chemotaxis of human breast cancer cells. In this study, we investigated the role of PKCζ in CSF‐1‐induced chemotaxis of macrophages. Knockdown of PKCζ by small interference RNA impaired CSF‐1‐induced chemotaxis of human acute monocytic leukemia cell line THP‐1, which was probably a result of a decrease in CSF‐1‐induced phosphorylation of LIN‐11, Is11, and MEC‐3 protein domain kinase (LIMK)/cofilin and actin polymerization. Furthermore, silencing PKCζ expression also impaired migration of mouse peritoneal macrophages. Scratch analysis indicated that PKCζ was required for macrophage migration. Therefore, PKCζ is required for CSF‐1‐induced chemotaxis of macrophages. Blocking activation of PKCζ will be a novel strategy to inhibit cancer metastasis by blocking migration of cancer cells and macrophages.